Notice of Pre-AIA or AIA Status
The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
DETAILED ACTION
1. Applicant’s response filed on June 30, 2026 is acknowledged. Claims 39-68 are currently pending. Claims 39, 42-43, 53 and 56 have been amended. Claim 52 was previously withdrawn from consideration as being drawn to a non-elected invention. Claims 39-51 and 53-68 are currently under examination.
Objections Withdrawn
2. In view of Applicant’s amendment, the objection to claim 42 for a grammatical informality is withdrawn.
Rejections Withdrawn
3. In view of Applicant’s amendment, the rejection of claim 56 under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as being indefinite for failing to particularly point out and distinctly claim the subject matter which the inventor or a joint inventor (or for applications subject to pre-AIA 35 U.S.C. 112, the applicant), regards as the invention by the use of the phrase “wherein said administration comprises locating the cricoid cartilage of the larynx to identify the location of the stellate ganglion’ is withdrawn.
Objection Maintained
Claim Objections
4. The objection to claims 49 and 65 because said claims depends upon a rejected based claim is maintained for the reasons previously stated. Appropriate correction is required.
Rejections Maintained
Claim Rejections - 35 USC § 102
The following is a quotation of the appropriate paragraphs of 35 U.S.C. 102 that form the basis for the rejections under this section made in this Office action:
A person shall be entitled to a patent unless –
(a)(1) the claimed invention was patented, described in a printed publication, or in public use, on sale, or otherwise available to the public before the effective filing date of the claimed invention.
(a)(2) the claimed invention was described in a patent issued under section 151, or in an application for patent published or deemed published under section 122(b), in which the patent or application, as the case may be, names another inventor and was effectively filed before the effective filing date of the claimed invention.
5. The rejection of claim(s) 39-47, 50, 51, 53-55, 57, 61-63, and 66-68 under 35 U.S.C. 102(a)(1)/102(a)(2) as being anticipated by Carroll et al., US 2007/0264373 A1; Published: Nov. 15, 2007 is maintained for the reasons set forth in the previous office action.
Independent claim 39 is drawn to a method of treating a cardiovascular disorder comprising: administering a botulinum toxin into the stellate ganglion of a mammal to treat at least one of angina, arrhythmias of heart rate, a myocardial contractility disorder, coronary artery disease, and high blood pressure; thereby reducing the occurrence of at least one symptom of the disorder, wherein said administration comprises a total dose per year of not more than 400 Units of the botulinum toxin.
Independent claims 42 is drawn to a method of treating a cardiovascular disorder comprising: administering a botulinum toxin into the stellate ganglion in a subject with a cardiovascular disorder to thereby treat their symptoms, wherein said administration comprises a total dose per year of not more than 400 Units of the botulinum toxin.
Independent claim 43 is drawn to a method of treating a cardiovascular disorder comprising administering a botulinum toxin into the stellate ganglion wherein the administration is performed by imaging the treatment area, wherein said administration comprises a total dose per year of not more than 400 Units of the botulinum toxin.
Independent claim 53 is drawn to a method of treating a cardiovascular disorder comprising the steps of administering a botulinum toxin into the stellate ganglion nerve of a mammal to treat at least one of arrhythmias of heart rate, a myocardial contractility disorder, coronary artery disease, and high blood pressure; and administering a local anesthetic to the stellate ganglion nerve of said mammal, thereby reducing the occurrence of at least one symptom of the disorder, wherein said administration comprises a total dose per year of not more than 400 Units of the botulinum toxin.
Carroll discloses methods to extend sympathetic nerve block, by administration of a neurotoxin at and/or around a targeted sympathetic ganglion. A preferred neurotoxin is a botulinum toxin, e.g. serotypes A, B, C1, D, E, F and G. The neurotoxin may be administered percutaneously as one or a cocktail of serotypes; and is optionally combined with a local anesthetic, anti-inflammatory agent, and the like (see paragraph 0019; meets limitations of claim 39, 42-43, 54 and 68).
In one embodiment of the invention, the toxin used to induce sympathetic block is used for the treatment of sympathetically maintained pain. In this method, the involvement of sympathetic nerves may be initially diagnosed through a short-term sympathetic block, for example by administration of an IV adrenergic antagonist; percutaneous administration of local anesthetic near the sympathetic ganglion or chain, and the like. Following confirmation of sympathetic involvement in pain, the neurotoxin is administered to the targeted sympathetic ganglion (see paragraph 0020; meets limitations of claim 39, 42-43 and 68). In one embodiment, a block of the upper extremities is established by administration of neurotoxin to the stellate ganglion, i.e. affecting the inferior, middle and superior cervical sympathetic nerves (see paragraph 0021; meets limitations of claim 39, 42-43 and 68).
Moreover, the toxin induced sympathetic block is used to treat cardiovascular conditions that are improved by an interruption of sympathetic stimulation, e.g. hypertension, and other conditions where sympathetically induced vasoconstriction adversely affects a patient's health. In yet another embodiment, the toxin induced sympathetic block is used to treat conditions characterized by smooth muscle spasms, some of which smooth muscles may be arterial, e.g. in the treatment of cerebral vasospasm, coronary vasospasm, peripheral vasospasm and the like (see paragraph 0022; meets claims 42, 51, 53, and 67). Further, the botulinum toxin is botulinum toxin type A. In a preferred embodiment, the botulinum toxin is administered as a complex, in order to enhance the stability of the toxin (see paragraph 0032; meets claims 40, 44 and 55). The effective dose is from about 1 to 300 units (see claim 3; meets claims 45-47 and 61-63).
Carroll discloses that treatment with an analgesically effective dose of toxin is performed by injection of the dose in the retroperitoneal space at the border of the ganglion or vertebral body. The injection may be performed with a single or divided dose. Fluoroscopic guidance may be used to aid in the procedure (see paragraph 0056; meets claims 41, 43 and 57). Further, the term “unit dosage forms” refers to physically discrete units suitable as unitary dosages for a human subject. Each unit contains a predetermined quantity of active material calculated to produce the desired onset, tolerability, and therapeutic effects, in association with a suitable pharmaceutical excipient (e.g., an ampoule) (see paragraph 0037; meets limitation of claims 45-47 and 61-63). Anesthetics of interest for the methods of the invention include lidocaine. These agents are used at conventional doses, as known in the art (see paragraph 0044; meets claims 53-54). The toxin may be administered as a pharmaceutical formulation of one or a combination of toxins and may further comprise a corticosteroid routinely administered orally or by injection. In another embodiment, the pharmaceutical formulation further comprises a local anesthetic, as described above (see paragraph 0049; meets claim 53).
Lastly, other cardiovascular conditions can be related to atherosclerosis, e.g. coronary artery disease, which may be aided with a block of the sympathetic trunk; and post prandial ischemia, which may be aided by a celiac plexus block. Additional cardiovascular conditions include essential hypertension, which may be aided with a block of the sympathetic ganglion in the celiac plexus, aortorenal ganglion; lumbar sympathetic ganglion; and celiac ganglion (see paragraph 0060; meets claims 50, 66 and 68).
Applicant argues that:
1) To expedite prosecution the rejected independent claims are amended herein to specify “said administration comprises a total dose per year of not more than 400 Units of the botulinum toxin.”
Applicant’s arguments have been fully considered and are deemed non-persuasive.
With regard to Point 1, the method of Carroll is identical to that of the method as claimed. Carroll discloses a method of treating a cardiovascular disorder comprising administering an effective dose of from about 1 to 300 units of botulinum toxin into the stellate ganglion of a mammal to treat at least one of angina, arrhythmias of heart rate, a myocardial contractility disorder, coronary artery disease, and high blood pressure; thereby reducing the occurrence of at least one symptom of the disorder.
The Office takes the position that if the method of Carroll is performed one time, which by all appearances it is, it would be a total dose per year of not more than 400 Units of the botulinum toxin. Therefore, the Office takes the position that taken as a whole Carroll remains anticipatory of the invention as claimed. Thus, the rejection is thereby maintained for the reasons set forth in the previous Office action.
6. The rejection of claim(s) 39-48, 51, 58 and 59 under 35 U.S.C. 102(a)(1) as being anticipated by Yu et al., Heart Rhythm, 2019;16(5): supp. S-PO05-059 is maintained for the reason set forth in the previous office action.
Independent claim 39 is drawn to a method of treating a cardiovascular disorder comprising: administering a botulinum toxin into the stellate ganglion of a mammal to treat at least one of angina, arrhythmias of heart rate, a myocardial contractility disorder, coronary artery disease, and high blood pressure; thereby reducing the occurrence of at least one symptom of the disorder, wherein said administration comprises a total dose per year of not more than 400 Units of the botulinum toxin.
Independent claims 42 is drawn to a method of treating a cardiovascular disorder comprising: administering a botulinum toxin into the stellate ganglion in a subject with a cardiovascular disorder to thereby treat their symptoms, wherein said administration comprises a total dose per year of not more than 400 Units of the botulinum toxin.
Independent claim 43 is drawn to a method of treating a cardiovascular disorder comprising administering a botulinum toxin into the stellate ganglion wherein the administration is performed by imaging the treatment area, wherein said administration comprises a total dose per year of not more than 400 Units of the botulinum toxin.
Yu et al. disclose that stellate ganglion suppression has been shown to prevent ventricular arrhythmias (VAs). Botulinum toxin type A (BTA) is a typical neurotoxin that can effectively block the ganglion. Further, Yu discloses that their method uses ultrasound guided percutaneous microinjection of BTA to block the left stellate ganglion (LSG) and prevent ischemia-induced VAs. Specifically, 50U/0.25ml BTA was microinjected into LSG percutaneously under the guidance of ultrasound. Compared with the control group, BTA significantly inhibited LSG function and neural activity, and prolonged ventricular ERP from 3 hours up to 5 hours post-BTA microinjection. Particularly, BTA microinjection into LSG significantly suppressed ischemia-induced VAs. The ischemia-induced nerve growth factor and c-fos overexpression were also significantly down-regulated by BTA. In addition, the tunnel staining showed no significant difference between the two groups. In conclusion, ultrasound-guided percutaneous microinjection of BTA could block LSG neural activity and prevent the ischemia induced Vas (see all of S-PO05-059; meets claims 39-48 and 58).
As it pertains to claim 51, the method steps as claimed are identical to that of the prior art, the cardiovascular disorder, absent evidence to the contrary, necessarily comprises high blood pressure, which are closely linked, as high blood pressure caused structural changes in the heart that trigger fast-paced rhythm abnormalities as well as the fact that an increase in blood pressure, by any means, can induce ventricular arrhythmias.
As it pertains to claim 59, Yu discloses the treatment of arrhythmias of heart rate, the method steps are identical and therefore, absent evidence to the contrary, treating arrhythmia necessarily comprises stabilizing ventricular rhythm or reducing tachycardia symptoms.
Applicant argues that:
1) To expedite prosecution the rejected independent claims are amended herein to specify “said administration comprises a total dose per year of not more than 400 Units of the botulinum toxin.”
Applicant’s arguments have been fully considered and are deemed non-persuasive.
With regard to Point 1, the method of Yu is identical to that of the method as claimed. Yu discloses that stellate ganglion suppression has been shown to prevent ventricular arrhythmias (VAs). Botulinum toxin type A (BTA) is a typical neurotoxin that can effectively block the ganglion. Further, Yu discloses that their method uses ultrasound guided percutaneous microinjection of BTA to block the left stellate ganglion (LSG) and prevent ischemia-induced VAs. Specifically, 50U/0.25ml BTA was microinjected into LSG percutaneously under the guidance of ultrasound.
The Office takes the position that if the method of Carroll is performed one time, which by all appearances it is, it would be a total dose per year of not more than 400 Units of the botulinum toxin. Therefore, the Office takes the position that taken as a whole Carroll remains anticipatory of the invention as claimed. Thus, the rejection is thereby maintained for the reasons set forth in the previous Office action.
Claim Rejections - 35 USC § 103
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
7. The rejection of claim(s) 56 under 35 U.S.C. 103 as being unpatentable over Carroll et al., US 2007/0264373 A1; Published: Nov. 15, 2007 is maintained for the reasons set forth in the previous office action.
The following rejection has been updated to address the amendments as filed.
Dependent claim 56 is drawn to a method a claimed wherein said administration comprises locating the cricoid cartilage of the larynx to identify the location of the stellate ganglion and injecting the botulinum toxin and the local anesthetic into the stellate ganglion or vicinity thereof.
Carroll teaches methods to extend sympathetic nerve block, by administration of a neurotoxin at and/or around a targeted sympathetic ganglion. A preferred neurotoxin is a botulinum toxin, e.g. serotypes A, B, C1, D, E, F and G. The neurotoxin may be administered percutaneously as one or a cocktail of serotypes; and is optionally combined with a local anesthetic, anti-inflammatory agent, and the like (see paragraph 0019; meets limitations of claim 39, 42-43 and 68).
In one embodiment of the invention, the toxin used to induce sympathetic block is used for the treatment of sympathetically maintained pain. In this method, the involvement of sympathetic nerves may be initially diagnosed through a short term sympathetic block, for example by administration of an IV adrenergic antagonist; percutaneous administration of local anesthetic near the sympathetic ganglion or chain, and the like. Following confirmation of sympathetic involvement in pain, the neurotoxin is administered to the targeted sympathetic ganglion (see paragraph 0020; meets limitations of claim 39, 42-43 and 68). In one embodiment, a block of the upper extremities is established by administration of neurotoxin to the stellate ganglion, i.e. affecting the inferior, middle and superior cervical sympathetic nerves (see paragraph 0021; meets limitations of claim 39, 42-43 and 68).
Moreover, Carroll teaches that the toxin induced sympathetic block is used to treat cardiovascular conditions that are improved by an interruption of sympathetic stimulation, e.g. hypertension, and other conditions where sympathetically induced vasoconstriction adversely affects a patient's health. In yet another embodiment, the toxin is induced sympathetic block is used to treat conditions characterized by smooth muscle spasms, some of which smooth muscles may be arterial, e.g. in the treatment of cerebral vasospasm, coronary vasospasm, peripheral vasospasm and the like (see paragraph 0022; meets claims 42, 51, 53, and 67). Further, the botulinum toxin is botulinum toxin type A. In a preferred embodiment, the botulinum toxin is administered as a complex, in order to enhance the stability of the toxin (see paragraph 0032; meets claims 40, 44 and 55).
Further, Carroll teaches that the botulinum toxins for use according to the present invention may be provided in liquid form or can be stored in lyophilized or vacuum dried form in containers under vacuum pressure. The lyophilized or vacuum dried material can be reconstituted with saline or water, or local anesthetic or other medicine that do not degrade the Botulinum toxin, and may produce an independent neuromodulatory effect (see paragraph 0033; meets a limitation of claim 56). The effective dose is from about 1 to 300 units (see claim 3; meets claims 45-47 and 61-63). Treatment with an analgesically effective dose of toxin is performed by injection of the dose in the retroperitoneal space at the border of the ganglion or vertebral body. The injection may be performed with a single or divided dose. Fluoroscopic guidance may be used to aid in the procedure (see paragraph 0056; meets claims 41, 43 and 57).
The term “unit dosage forms” refers to physically discrete units suitable as unitary dosages for a human subject. Each unit contains a predetermined quantity of active material calculated to produce the desired onset, tolerability, and therapeutic effects, in association with a suitable pharmaceutical excipient (e.g., an ampoule) (see paragraph 0037; meets limitation of claims 45-47 and 61-63). Anesthetics of interest for the methods of the invention include lidocaine. These agents are used at conventional doses, as known in the art (see paragraph 0044; meets claims 53-54). The toxin may be administered as a pharmaceutical formulation of one or a combination of toxins and may further comprise a corticosteroid routinely administered orally or by injection. In another embodiment, the pharmaceutical formulation further comprises a local anesthetic, as described above (see paragraph 0049; meets claim 53).
Lastly, other cardiovascular conditions can be related to atherosclerosis, e.g. coronary artery disease, which may be aided with a block of the sympathetic trunk; and post prandial ischemia, which may be aided by a celiac plexus block. Additional cardiovascular conditions include essential hypertension, which may be aided with a block of the sympathetic ganglion in the celiac plexus, aortorenal ganglion; lumbar sympathetic ganglion; and celiac ganglion (see paragraph 0060; meets claims 50, 66 and 68).
Carroll do not specifically teach that their administration comprises locating the cricoid cartilage of the larynx to identify the location of the stellate ganglion and injecting into the stellate ganglion or vicinity thereof.
It would have been obvious before the effective filing date of the presently claimed invention to locate the cricoid cartilage of the larynx to identify the location of the stellate ganglion and then inject into the stellate ganglion or vicinity thereof with a reasonable expectation of success because it is obvious to one of ordinary skill in the art to use fluoroscopy to locate the cricoid cartilage of the larynx to identify properly the location of the stellate ganglion. The skilled artisan would have been motivated to make this modification because of the prior art teaches (at paragraph 0056) that the injection may be performed with a single or divided dose and that Fluoroscopic guidance may be used to aid in the procedure.
Accordingly, the subject matter of claim 56 would have been prima facie obvious to one of ordinary skill in the art before the effective filing date of the presently claimed invention, absent evidence to the contrary.
Applicant argues that:
1) Applicant traverses the rejection. Nevertheless, Applicant has amended independent claim 53 (from which claim 56 depends) to specify “said administration comprises a total dose per year of not more than 400 Units of the botulinum toxin.” This element is not taught or suggested by the prior art.
Applicant’s arguments have been fully considered and are deemed non-persuasive.
With regard to Point 1, as discussed above, Carroll teaches the method as claimed. The Office maintains the position that if the method of Carroll is performed one time, which by all appearances it has been, it would be a total dose per year of not more than 400 Units of the botulinum toxin. Therefore, Carroll remains an appropriate obvious rejection and the rejection is maintained.
8. The rejection of claim(s) 53-64 and 67 under 35 U.S.C. 103 as being unpatentable over Yu et al., Heart Rhythm, 2019;16(5): supp. S-PO05-059 as applied to claims 39-48, 51 and 58 above, and further in view of Tian et al., Circ Arrhythm Electrophysiol., 2019; 12(e007118):1-8; and evidenced by Piraccini et al., Stellate Ganglion Blocks, NCBI Bookshelf, 2023; StatPears [Internet] is maintained for the reasons set forth in the previous office action.
Yu teaches that stellate ganglion suppression has been shown to prevent ventricular arrhythmias (VAs). Botulinum toxin type A (BTA) is a typical neurotoxin that can effectively block the ganglion. Further, Yu discloses that their method uses ultrasound guided percutaneous microinjection of BTA to block the left stellate ganglion (LSG) and prevent ischemia-induced VAs. Specifically, 50U/0.25ml BTA was microinjected into LSG percutaneously under the guidance of ultrasound. Compared with the control group, BTA significantly inhibited LSG function and neural activity, and prolonged ventricular ERP from 3 hours up to 5 hours post-BTA microinjection. Particularly, BTA microinjection into LSG significantly suppressed ischemia-induced VAs. The ischemia-induced nerve growth factor and c-fos overexpression were also significantly down-regulated by BTA. In addition, the tunnel staining showed no significant difference between the two groups. In conclusion, ultrasound-guided percutaneous microinjection of BTA could block LSG neural activity and prevent the ischemia induced Vas (see all of S-PO05-059; meets claims 39-48 and 58).
As it pertains to claim 51, the method steps as claimed are identical to that of the prior art, the cardiovascular disorder, absent evidence to the contrary, necessarily comprises high blood pressure, which are closely linked, as high blood pressure caused structural changes in the heart that trigger fast-paced rhythm abnormalities as well as the fact that an increase in blood pressure, by any means, can induce ventricular arrhythmias.
As it pertains to claim 59, Yu discloses the treatment of arrhythmias of heart rate, the method steps are identical and therefore, absent evidence to the contrary, treating arrhythmia necessarily comprises stabilizing ventricular rhythm or reducing tachycardia symptoms.
Yu does not specifically teach an administration of a local anesthetic to the stellate ganglion nerve, as recited in claim 53 or that said local anesthetic comprises lidocaine, as recited in claim 54; nor does it specifically teach imaging comprising fluoroscopy or ultrasound, as recited in claims 57-58.
Tian teaches that bupivacaine, alone or combined with lidocaine, was injected into the neck with good local anesthetic spread in the vicinity of the left stellate ganglion or both stellate ganglia. Percutaneous SGB may be considered for stabilizing ventricular rhythm in patients for whom other therapies have failed. Ventricular arrhythmia (VA) is a common and potentially lethal clinical event in patients with or without heart disease. Clustered episodes of ventricular tachycardia (VT) or ventricular fibrillation (VF), also known as electrical storm (ES)Studies showed that the autonomic nervous system has an important role in the triggering and maintenance of VA,4,5 especially in ES.3 Therefore, suppressing sympathetic activity may be imperative for controlling VA. The burden of VA may be reduced by cardiac sympathetic intervention by unilateral left or bilateral stellate ganglion blockade (SGB) through pharmacological infiltration or by left cardiac sympathetic denervation through surgical resection of the extrinsic sympathetic chain. Urgent surgical left cardiac sympathetic denervation, however, is difficult to perform in patients with ES. Ultrasound-guided percutaneous SGB—a bedside procedure—is an alternative and possibly effective therapy for the management of ES (see abstract and page 2).
Further, Tian teaches that during the SGB procedure the operator can make the decision to use ultrasonography guided or fluoroscopy-guided SGB, and the anesthesiologist and clinician caring for the patient makes the decision to perform unilateral or bilateral SGB (see page 2; SGB Procedure). All pertinent structures were identified by ultrasonography (carotid artery, left internal jugular vein, longus coli muscle, vertebral artery, anterior scalene muscle, and brachial plexus). The skin was anesthetized with 2 mL of 1% lidocaine. A 22-gauge, 2-inch spinal needle (Pajunk) was advanced in-plane in a posterior-to-anterior direction to the anterior surface of the longus coli muscle to avoid all vascular structures. After a negative aspiration, local anesthetic agents were injected incrementally. The stellate ganglion was visualized lifting off the anterior aspect of the longus coli muscle (Figure 1) (see page 3; Ultrasonography-Guided SGB).
The anterolateral points of entry on the skin, targeting the uncinate processes of C6 bilaterally, were infiltrated using 1% lidocaine. Care was taken to avoid puncturing any preexisting appliances in the neck. Under fluoroscopic guidance, a 3.5-inch, 25-gauge spinal needle was advanced to gently contact the uncinate process/base of the trans verse process. After a negative aspiration, 0.5 mL of contrast media was injected, which had to show a nonvascular spread pattern in the region of the stellate ganglion. Next, local anesthetic agents were slowly and incrementally injected after frequent negative aspirations (see page 3; Fluoroscopy-Guided SGB). A total of 38 SGB procedures were performed in 30 patients (4 patients underwent 2 and 3 patients underwent 3 SGB procedures), of which 30 procedures were guided by ultrasound and 8 were guided by fluoroscopy. After the stellate ganglion was identified, the anesthetic agent was injected (Table 2)(see page 5; SGB Procedures).
As it pertains to claim 56, the Office takes the position that the use of the cricoid cartilage to identify the location of the stellate ganglion is a routine step in the claimed procedure as evidenced by Piraccini, which teaches that SGB is used for the treatment of many medical conditions including complex regional pain syndrome and peripheral vascular disease. Also noting that historically, the anesthetic has been injected at the C6 or C7 vertebral level with the Chassignac’s tubercle, the cricoid cartilage, and the carotid artery serving as the anatomic landmarks to the procedure (see continuing education activity).
It would have been obvious before the effective filing date of the presently claimed invention to employ a local anesthetic and imaging resources when administering botulinum toxin to or in the vicinity of the stellate ganglion in methods suggested by Yu et al. with a reasonable expectation of success. This modification may be viewed as a combining of elements known in the prior art where one skilled in the art could have combined the elements as claimed by known methods with no change in their respective functions, and the combination would have yielded predictable results to one of ordinary skill in the art at the time of the invention. See the recent Board decision Ex parte Smith,--USPQ2d--, slip op. at 20, (Bd. Pat. App. & Interf. June 25, 2007) (citing KSR, 82 USPQ2d at 1396).
The skilled artisan would have been motivated to make this modification because Tian suggests these particular steps, particularly, using ultrasound under fluoroscopic guidance-a bedside procedure- to identify the stellate ganglion and to ensure comfort, to see all pertinent structures, and to gently execute the procedure. Accordingly, the subject matter of the rejected claims would have been prima facie obvious to one of ordinary skill in the art before the effective filing date of the presently claimed invention, absent evidence to the contrary.
Applicant argues that:
1) Applicant traverses the rejection. Nevertheless, Applicant has amended independent claim 53 (from which claim 56 depends) to specify “said administration comprises a total dose per year of not more than 400 Units of the botulinum toxin.” This element is not taught or suggested by the prior art.
Applicant’s arguments have been fully considered and are deemed non-persuasive.
With regard to Point 1, the method of Yu and Tian is identical to that of the method as claimed. They disclose a method of treating a cardiovascular disorder comprising administering an effective dose of 50U/0.25ml BTA. Moreover, the Office maintains the position that if the method of Yu and Tian is performed one time, which by all appearances it has been, it would be a total dose per year of not more than 400 Units of the botulinum toxin. Therefore, Carroll remains an appropriate obvious rejection and the rejection is maintained.
Conclusion
9. No claim is allowed.
10. Applicant's amendment necessitated the new ground(s) of rejection presented in this Office action. Accordingly, THIS ACTION IS MADE FINAL. See MPEP § 706.07(a). Applicant is reminded of the extension of time policy as set forth in 37 CFR 1.136(a).
A shortened statutory period for reply to this final action is set to expire THREE MONTHS from the mailing date of this action. In the event a first reply is filed within TWO MONTHS of the mailing date of this final action and the advisory action is not mailed until after the end of the THREE-MONTH shortened statutory period, then the shortened statutory period will expire on the date the advisory action is mailed, and any nonprovisional extension fee (37 CFR 1.17(a)) pursuant to 37 CFR 1.136(a) will be calculated from the mailing date of the advisory action. In no event, however, will the statutory period for reply expire later than SIX MONTHS from the mailing date of this final action.
11. Any inquiry concerning this communication or earlier communications from the examiner should be directed to LAKIA J JACKSON-TONGUE whose telephone number is (571)272-2921. The examiner can normally be reached Monday-Friday 930AM-530PM.
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If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Anne Gussow can be reached at (571) 272-6047. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
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/LAKIA J JACKSON-TONGUE/Examiner, Art Unit 1645 August 31, 2026
/BRIAN GANGLE/Primary Examiner, Art Unit 1645
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